title: IL-6 trans-signaling enhances CCL20 production from IL-1β-stimulated human periodontal ligament cells.
abstract: CC chemokine ligand 20 (CCL20) plays a central role in the recruitment of CCR6-expressing cells, including Th17 cells which are related to bone resorption in periodontal lesions and thus in the development of periodontal disease. IL-6 is an important cytokine that is associated with the pathogenesis of periodontitis. However, the effect of IL-6 on CCL20 production is uncertain. The aim of this study was to examine whether IL-6 could modify CCL20 expression in human periodontal ligament cells (HPDLCs). HPDLCs expressed gp130 but did not express IL-6R on the surface of HPDLCs. So, IL-6 trans-signaling is important to recognize IL-6 by HPDLCs. IL-6/sIL-6R stimulation enhanced CCL20 production in IL-1β-stimulated HPDLCs. IL-6 produced from IL-1β-stimulated HPDLCs with sIL-6R could increase CCL20 production in HPDLCs with sIL-6R. Signal transducer and activator of transcription (STAT)3 activation was related to CCL20 production in IL-1β and IL-6/sIL-6R-stimulated HPDLCs. Our data suggests that HPDLCs, in response to IL-6, sIL-6R, and IL-1β, may shift chemokine production to that favoring CCR6-expressing cells recruitment in periodontal lesions.
authors.affiliation: Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan, hosokawa@tokushima-u.ac.jp.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Hosokawa
authors.forename: Satoru
authors.initials: S
authors.lastname: Shindo
authors.forename: Ikuko
authors.initials: I
authors.lastname: Hosokawa
authors.forename: Kazumi
authors.initials: K
authors.lastname: Ozaki
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsuo
mesh_terms: D002478:Cells, Cultured; D054418:Chemokine CCL20 / Q000378:metabolism*; D050822:Cytokine Receptor gp130 / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism* / Q000494:pharmacology; D015850:Interleukin-6 / Q000378:metabolism* / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D010513:Periodontal Ligament / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D010518:Periodontitis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019947:Receptors, Interleukin-6 / Q000378:metabolism; D011994:Recombinant Proteins / Q000494:pharmacology; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D015854:Up-Regulation
chemical_list: C108355:CCL20 protein, human; D054418:Chemokine CCL20; C508600:IL6 protein, human; C508603:IL6R protein, human; C494199:IL6ST protein, human; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D016328:NF-kappa B; D019947:Receptors, Interleukin-6; D011994:Recombinant Proteins; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D050822:Cytokine Receptor gp130; D020928:Mitogen-Activated Protein Kinases